0
We're unable to sign you in at this time. Please try again in a few minutes.
Retry
We were able to sign you in, but your subscription(s) could not be found. Please try again in a few minutes.
Retry
There may be a problem with your account. Please contact the AMA Service Center to resolve this issue.
Contact the AMA Service Center:
Telephone: 1 (800) 262-2350 or 1 (312) 670-7827  *   Email: subscriptions@jamanetwork.com
Error Message ......
Clinicopathologic Reports, Case Reports, and Small Case Series |

Macular Infarction Following Viperine Snake Bite FREE

Jatinder Singh, MS, DNB; Preetam Singh, DOMS; Rajbir Singh, MS; Vipin Kumar Vig, MS
[+] Author Affiliations

Section Editor: W. Richard Green, MD

More Author Information
Arch Ophthalmol. 2007;125(10):1430-1431. doi:10.1001/archopht.125.10.1430.
Text Size: A A A
Published online

Macular infarction has been reported following toxic influences, for example, aminoglycoside toxicity.1 Venomous snake bites may result in neurologic or hemostatic dysfunction. Viperine (hemotoxic) snake bites may produce coagulopathy, which may result in several systemic complications. Ocular involvement is rare. Common ocular problems encountered after a snake bite are generally neurologic (ptosis, ophthalmoplegia, accommodation paralysis, and optic neuritis). Visual loss may result from direct inoculation of venom into the eye (globe necrosis, keratomalacia, and uveitis), from optic neuritis, or secondary to hemostatic abnormality (vitreous hemorrhage, cortical infarction, and central retinal artery occlusion).25

REPORT OF A CASE

A 17-year-old girl was bitten by a viperine snake. She was admitted to a local hospital in an unconscious state and administered first aid, anti–snake venom serum, and supportive care. She regained consciousness 14 hours after the snake bite and 6 hours later reported loss of vision in her left eye. She came to us 5 days later. Visual acuity was recorded as 20/20 OD and no light perception OS. Ophthalmological examination disclosed unremarkable anterior segment and normal intraocular pressures in both eyes. Relative afferent pupillary defect was observed in the left eye. Fundus examination revealed optic disc hyperemia, splinter-shaped hemorrhages at the posterior pole, and a cherry-red spot at the center of the macula (Figure 1). Fluorescein angiography demonstrated normal arm-retina (10-second) and arteriovenous transit (11-second) times. Blocked choroidal fluorescence was observed in relation to the nerve fiber layer hemorrhages. The most striking feature on fluorescein angiography was pruning of the perifoveal capillaries. The silhouette of occluded macular capillaries was observed against the choroidal flush. Late-phase angiograms showed optic disc staining (Figure 2).

Place holder to copy figure label and caption
Figure 1.

Fundus photograph showing a cherry-red spot at the macula and superficial retinal hemorrhages.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 2.

Early (A) and late phase (B) fluorescein angiograms demonstrate pruning of the perifoveal capillaries and optic disc staining, respectively.

Graphic Jump Location

Systemic examination revealed no deficit. Laboratory investigations showed mild anemia (hemoglobin level, 10.4 g/dL [to convert to grams per liter, multiply by 10.0]), leukocytosis (13 800/μL [to convert to ×109 per liter, multiply by 0.001]), and neutrophilia (74%). Results of renal function tests, abdominal ultrasonography, electrocardiography, echocardiography, and magnetic resonance imaging of the brain were normal. Dual antiplatelet therapy (aspirin, 75 mg/d, and clopidogrel, 75 mg/d), systemic antibiotics, and oral prednisone (40 mg/d tapered by 10 mg/wk) were started. Three months later, the visual acuity remained no light perception. Optic disc pallor and gross attenuation of perifoveal vessels were noted. The macula showed pigment clumping and atrophy (Figure 3).

Place holder to copy figure label and caption
Figure 3.

At 3-month follow-up, coarse pigment clumping and atrophy at the macula and gross attenuation of the macular arterioles are evident. Note also the optic disc pallor.

Graphic Jump Location

COMMENT

Snake venom is a complex heterogeneous composition of substances that predominantly affects the synapse (neurotoxic) or coagulation pathway (hemotoxic). Large doses can result in disseminated intravascular coagulopathy (DIC) and ischemic damage to vital organs. Toxic vasculitis has reportedly been caused by certain species of the Viperidae family.5 Hemorrhagins (complement-mediated toxic components of viperine venom) may induce severe vasospasm, endothelial damage, and increased vascular permeability. Vasospasm and/or DIC may result in vascular occlusion. Fibrin thrombi in the capillaries, perivascular hemorrhages, and necrosis, all observed in our patient, are features of DIC.

The likely cause of visual loss could be (1) ophthalmic artery occlusion with subsequent dislodge of fibrin emboli into the end arterioles at the posterior pole; or (2) retinal necrosis and macular infarction secondary to an aborted DIC process associated with toxic optic neuropathy (venom or ASV serum toxicity).

Ocular complications following a snake bite range from keratomalacia to vitreous hemorrhage,4 uveitis, optic neuritis,3 globe necrosis, and visual loss due to cortical infarction.5 We are unaware of any previous report in the literature of macular infarction following a viperine snake bite. Visual prognosis is poor despite medical treatment.

ARTICLE INFORMATION

Correspondence: Dr Singh, Sardar Bahadur Dr Sohan Singh Eye Hospital, Katra Sher Singh, Chowk Farid, Amritsar-143006, Punjab, India (drjatinder@rediffmail.com).

Financial Disclosure: None reported.

REFERENCES

Campochiaro  PAConway  BP Aminoglycoside toxicity—a survey of retinal specialists: implications for ocular use. Arch Ophthalmol 1991;109 (7) 946- 950
PubMed Link to Article
Bhalla  AJain  APBanait  S  et al.  Central retinal artery occlusion: an unusual complication of snake bite. J Venom Anim Toxins Incl Trop Dis 2004;10 (3) 311- 314
Link to Article
Menon  VTandon  RSharma  TGupta  A Optic neuritis following snake bite. Indian J Ophthalmol 1997;45 (4) 236- 237
PubMed
Rao  BM A case of bilateral vitreous haemorrhage following snake bite. Indian J Ophthalmol 1977;25 (2) 1- 2
PubMed
Merle  HDonnio  AAyeboua  L  et al.  Occipital infarction revealed by quadranopsia following snake bite by Bothrops lanceolatusAm J Trop Med Hyg 2005;73 (3) 583- 585
PubMed

Figures

Place holder to copy figure label and caption
Figure 1.

Fundus photograph showing a cherry-red spot at the macula and superficial retinal hemorrhages.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 2.

Early (A) and late phase (B) fluorescein angiograms demonstrate pruning of the perifoveal capillaries and optic disc staining, respectively.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 3.

At 3-month follow-up, coarse pigment clumping and atrophy at the macula and gross attenuation of the macular arterioles are evident. Note also the optic disc pallor.

Graphic Jump Location

Tables

References

Campochiaro  PAConway  BP Aminoglycoside toxicity—a survey of retinal specialists: implications for ocular use. Arch Ophthalmol 1991;109 (7) 946- 950
PubMed Link to Article
Bhalla  AJain  APBanait  S  et al.  Central retinal artery occlusion: an unusual complication of snake bite. J Venom Anim Toxins Incl Trop Dis 2004;10 (3) 311- 314
Link to Article
Menon  VTandon  RSharma  TGupta  A Optic neuritis following snake bite. Indian J Ophthalmol 1997;45 (4) 236- 237
PubMed
Rao  BM A case of bilateral vitreous haemorrhage following snake bite. Indian J Ophthalmol 1977;25 (2) 1- 2
PubMed
Merle  HDonnio  AAyeboua  L  et al.  Occipital infarction revealed by quadranopsia following snake bite by Bothrops lanceolatusAm J Trop Med Hyg 2005;73 (3) 583- 585
PubMed

Correspondence

CME
Also Meets CME requirements for:
Browse CME for all U.S. States
Accreditation Information
The American Medical Association is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The AMA designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 CreditTM per course. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Physicians who complete the CME course and score at least 80% correct on the quiz are eligible for AMA PRA Category 1 CreditTM.
Note: You must get at least of the answers correct to pass this quiz.
Please click the checkbox indicating that you have read the full article in order to submit your answers.
Your answers have been saved for later.
You have not filled in all the answers to complete this quiz
The following questions were not answered:
Sorry, you have unsuccessfully completed this CME quiz with a score of
The following questions were not answered correctly:
Commitment to Change (optional):
Indicate what change(s) you will implement in your practice, if any, based on this CME course.
Your quiz results:
The filled radio buttons indicate your responses. The preferred responses are highlighted
For CME Course: A Proposed Model for Initial Assessment and Management of Acute Heart Failure Syndromes
Indicate what changes(s) you will implement in your practice, if any, based on this CME course.

Multimedia

Some tools below are only available to our subscribers or users with an online account.

1,145 Views
10 Citations
×

Related Content

Customize your page view by dragging & repositioning the boxes below.

Articles Related By Topic
Related Collections
PubMed Articles
Jobs
JAMAevidence.com

The Rational Clinical Examination: Evidence-Based Clinical Diagnosis
Original Article: Does This Patient Have a Hemorrhagic Stroke?

The Rational Clinical Examination: Evidence-Based Clinical Diagnosis
Original Article: Does This Patient Have a Hemorrhagic Stroke?